Journal
SCIENCE
Volume 366, Issue 6467, Pages 881-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aav3487
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Funding
- Swiss National Science Foundation [130823, 146133, PP00P3_157448]
- Interdisciplinary Centre for Clinical Research (IZKF Wurzburg) [E-32]
- Bundesministerium fur Bildung und Forschung (BMBF) [FKZ 01ES0901, FKZ 01ES0802]
- Interdisciplinary Centre for Clinical Research [E-354]
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Myocarditis can develop into inflammatory cardiomyopathy through chronic stimulation of myosin heavy chain 6-specific T helper (T-H)1 and T(H)17 cells. However, mechanisms governing the cardiotoxicity programming of heart-specific T cells have remained elusive. Using a mouse model of spontaneous autoimmune myocarditis, we show that progression of myocarditis to lethal heart disease depends on cardiac myosin-specific T(H)17 cells imprinted in the intestine by a commensal Bacteroides species peptide mimic. Both the successful prevention of lethal disease in mice by antibiotic therapy and the significantly elevated Bacteroides-specific CD4(+) T cell and B cell responses observed in human myocarditis patients suggest that mimic peptides from commensal bacteria can promote inflammatory cardiomyopathy in genetically susceptible individuals. The ability to restrain cardiotoxic T cells through manipulation of the microbiome thereby transforms inflammatory cardiomyopathy into a targetable disease.
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